Effects of heart rate on ventricular size, stroke volume, and output in the normal human fetus: a prospective Doppler echocardiographic study.

Abstract

The effect of heart rate on cardiac output in the fetal heart is controversial. We used Doppler echocardiography to investigate the effects of increasing heart rate on stroke volume and ventricular output in the normal human fetal heart. Heart rate was increased in 25 human fetuses (mean age 36 weeks) by auditory stimulation with a sound emitter placed on the mother's abdomen. Aortic or pulmonary diameters were measured at valve level from two-dimensional echocardiographic images and cross-sectional areas were calculated. Blood flow velocity spectra from the pulmonary artery or aorta were digitized to obtain flow velocity integrals before and after auditory stimulation. Stroke volume was calculated as the product of the flow velocity integral and the area of the great vessel. Prestimulation mean heart rate was 132 + 8 beats/min and increased after auditory stimulation to 158 + 9 beats/min (p < .001). Stroke volume decreased with the increase in heart rate from 3.7 ± 1.4 ml before stimulation to 3.0 ± 1. 1 ml after stimulation (p < .001), but ventricular output calculated as the product of stroke volume and heart rate remained unchanged (0.48 0.18 liter/min before vs 0.48 + 0.17 liter/min after stimulation). The decrease in stroke volume was accompanied by a decrease in ventricular end-diastolic area, although there was no change either in end-systolic area or fractional change in area. This study demonstrates that increases in heart rate within the physiologic range in the normal human fetus result in a decrease in ventricular size and stroke volume but no We used Doppler echocardiography to measure stroke volume and ventricular output in the normal human fetus at rest and after increases in heart rate induced by auditory stimulation. Our purpose was to examine the relationship between heart rate and stroke volume in the normal fetus in an attempt to resolve the controversy regarding the regulatory effect of heart rate on cardiac output. This may have direct clinical relevance in predicting the effects of drugs with chronotropic activity currently used in the treatment of heart failure and arrhythmias in the human fetus.

Aberrances in Autonomic Cardiovascular Regulation in Fibromyalgia Syndrome and Their Relevance for Clinical Pain Reports

“…However, their magnitudes strongly depend on RRI. Lower RRI is associated with lower ventricular preload, which, mediated by the Frank-Starling mechanism, results in reduced SV (48). Consequently, the lower SV and LVET in FMS patients could be explained by their low RRI.…”

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“…In adults, the Frank-Starling mechanism refers to the direct influence of end-diastolic volume on stroke volume; the intrinsic length-tension relationship of increasing cardiac muscle length by increasing end-diastolic volume will increase contractile force and therefore increase stroke volume. Some fetal studies have demonstrated that heart rate is the major determinant of fetal cardiac output rather than stroke volume [46–48]. These studies found that increasing preload as a means of increasing stroke volume via blood or saline infusion had little effect on cardiac output [47].…”

Invited Lecture: Fetal cardiac function and circulatory dynamics—the impact of Doppler echocardiography

“…8 ' 9 In later investigations, however, Kenny and collaborators showed, using echo-Doppler technology, that variations in fetal heart rate were not necessarily associated with alterations in cardiac output. 10 Without delving into too many details, the following comments can be made on this controversial aspect of fetal myocardial function (Table 1). First, one must remember that the Frank-Starling relationship has been demonstrated in the isolated myocardium of the fetal heart.…”

“…45 while placental vascular impedance does not change during the same period. 10 This could decrease the amount of forward flow through the isthmus and create a growth discrepancy between this vascular segment and the adjacent arteries.…”